Evidence map›Paper›PMID 18996473›Full record

ReviewCellular signalling2009

Lysophosphatidic acid signaling in airway epithelium: role in airway inflammation and remodeling.

Yutong Zhao, Viswanathan Natarajan

Open access · greenAbstract readReview
In one paragraph

Review in Cellular signalling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.6field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 74 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Lysophospholipids in Lung Inflammatory Diseases.Advances in experimental medicine and biology · 2021
    Article
  12. Lipid Signaling in Ocular Neovascularization.International journal of molecular sciences · 2020
    Review
  13. Review
  14. Review
  15. Article
  16. Overexpression of acylglycerol kinase is associated with poorer prognosis and lymph node metastasis in nasopharyngeal carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  17. Review
  18. CARMA3 Is Critical for the Initiation of Allergic Airway Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  19. Spiroguanidine rhodamines as fluorogenic probes for lysophosphatidic acid.Chemical communications (Cambridge, England) · 2015
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Yutong ZhaoDepartment of Medicine, University of Chicago, Chicago, IL 60637, USA. yzhao@medicine.bsd.uchicago.edu
Viswanathan Natarajan
University of Chicago · US

Funding

Intracellular S1P &signaling in lung endothelial cellsR01HL079396 · NHLBI · UNIVERSITY OF CHICAGO · PI NATARAJAN, VISWANATHAN · 2005 to 2009
$1.8M
Protective Role of Intracellular S1P in Lung InjuryR37HL079396 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI NATARAJAN, VISWANATHAN · 2010 to 2010
$393k
NHLBI NIH HHS HL79396NHLBI NIH HHS R01 HL079396NHLBI NIH HHS R37 HL079396
6 · The paper itself

Abstract

Lysophosphatidic acid (LPA), a potent bioactive phospholipid, induces diverse cellular responses, including cell proliferation, migration, and cytokine release. LPA can be generated intracellularly and extracellularly through multiple synthetic pathways by action of various enzymes, such as phospholipase A(1/2) (PLA(1/2)), phospholipase D (PLD), acylglycerol kinase (AGK), and lysophospholipase D (lysoPLD). Metabolism of LPA is regulated by a family of lipid phosphate phosphatases (LPPs). Significant amounts of LPA have been detected in various biological fluids, including serum, saliva, and bronchoalveolar lavage fluid (BALF). The most significant effects of LPA appear to be through activation of the G-protein-coupled receptors (GPCRs), termed LPA(1-6). LPA regulates gene expression through activation of several transcriptional factors, such as nuclear factor-kappaB (NF-kappaB), AP-1, and C/EBPbeta. In addition to GPCRs, cross-talk between LPA receptors and receptor tyrosine kinases (RTKs) partly regulates LPA-induced intracellular signaling and cellular responses. Airway epithelial cells participate in innate immunity through the release of cytokines, chemokines, lipid mediators, other inflammatory mediators and an increase in barrier function in response to a variety of inhaled stimuli. Expression of LPA receptors has been demonstrated in airway epithelial cells. This review summarizes our recent observations of the role of LPA/LPA-Rs in regulation of airway epithelium, especially in relation to the secretion of pro- and anti-inflammatory mediators and regulation of airway barrier function.

Indexed as

AnimalsCytokinesEpithelial CellsGene Expression RegulationHumansInflammation MediatorsLysophospholipidsPhospholipasesPhosphoric Monoester HydrolasesReceptors, Lysophosphatidic AcidRespiratory MucosaSignal TransductionCytokinesInflammation Mediatorslysophosphatidic acidLysophospholipidsPhospholipasesPhosphoric Monoester HydrolasesReceptors, Lysophosphatidic Acid

Identifiers

PMID18996473
PMCPMC2660380
OpenAlexW1985336767

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.